English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Helicobacter pylori  is designated as a class I carcinogen of human gastric cancer following long-term infection. During this process,  H. pylori  bacteria persist in proliferation and death, and release bacterial components that come into contact with gastric epithelial cells and regulate host cell function. However, the impact of long-term exposure to  H. pylori  lysate on the pathological changes of gastric cells is not clear. In this study, we aimed to investigate the regulation and mechanisms involved in gastric cell dysfunction following continuous exposure to  H. pylori  lysate. We co-cultured gastric cell lines GES-1 and MKN-45 with  H. pylori  lysate for 30 generations, and we found that sustained exposure to  H. pylori  lysate inhibited GES-1 cell invasion, migration, autophagy, and apoptosis, while it did not inhibit MKN-45 cell invasion or migration. Furthermore, Mongolian gerbils infected with  H. pylori  ATCC 43504 strains for 90 weeks confirmed the  in vitro  results. The clinical and  in vitro  data indicated that sustained exposure to  H. pylori  lysate inhibited cell apoptosis and autophagy through the  Nod1-NF-κB/MAPK-ERK/FOXO4  signaling pathway. In conclusion, sustained exposure to  H. pylori  lysate promoted proliferation of gastric epithelial cells and inhibited autophagy and apoptosis  via Nod1-NF-κB/MAPK-ERK/FOXO4  signaling pathway. In the process of  H. pylori- induced gastric lesions,  H. pylori  lysate plays as an “accomplice” to carcinogenesis.

Sustained Exposure to Helicobacter pylori Lysate Inhibits Apoptosis and Autophagy of Gastric Epithelial Cells